Respiratory response to CO2 by controlled alveolar hypercapnia

A method of assessing the respiratory response to a hypercapnic stimulus after an increase in alveolar pCO₂ in accordance with an assigned program is suggested. The results are independent of the metabolic level, resistance to respiration, and other factors. Unlike the widely used rebreathing method, this new method enables the ventilatory sensitivity to CO₂ to be compared at rest, during muscular work, when the resistance to respiration is changed, and so on. It can also be used for both clinical and experimental investigations.Respiratory Physiology Group, I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Chernigovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 89, No. 1, pp. 6–7, January, 1980.     

Nitric oxide (NO) in expired air at rest and during exercise

Nitric oxide (NO) was analysed in expired air from 27 healthy human subjects. At rest the NO concentration was 10.5 ± 0.9 ng 1^-1 (mean ± SEM) corresponding to 8.6 ± 0.7 parts per billion (ppb). The expired NO concentration did not change when the subjects were switched from breathing NO-free tank gas to room air which contained 7.7 ng 1^-1 NO. Repeated measurements of expired NO with an interval of 1 day showed a mean variation of 2.2 ± 0.7ngl^-1 NO. The NO concentration in the first portion in the expired tidal volume (44%) was insignificantly higher than in the latter expired portion, 6.9 ± 1.9 vs. 5.1 ± 1.0 ng 1^-1 (n= 5). During moderately heavy exercise on an ergometer bicycle (90 W for women, n= 4, 150 W for men, n= 4) the expired concentration of NO decreased, however because of increased minute ventilation, the expired amount of NO almost doubled (from 111 ± 12 to 209 ± 30 ng min^-1). The source of the expired NO is not clear and both the airways and the pulmonary circulation may contribute.     

Interaction of peripheral and central respiratory drives in cats I. Effects of sodium cyanide as a peripheral chemoreceptor stimulus at different levels of CSF pH

In cats anesthetized with chloralose-urethane, the central respiratory chemoreceptors were exposed to mock CSF of pH 7.02, 7.20, or 7.57. The right carotid body was simultaneously stimulated by intracarotid injections of 40, 80, or 160 μg sodium cyanide in 200 μl Ringer solution. The left carotid nerve and, in some animals, both vagosympathetic truncs were dissected. It could be demonstrated the the increase in ventilation produced by application of NaCN to the peripheral chemoreceptors is significantly larger at high than at low mock CSF pH (i.e. at low than at high central stimulus intensity). In vagotomized cats the responses of V_T and gelai to NaCN similarly depend upon CSF pH; they are somewhat larger, though, than in intact animals. These results are discussed as compared with results reported by different authors. Supported by the Deutsche Forschungsgemeinschaft (Be 477)     

轻度过度通气下施行CO2气腹对呼吸和动脉血气的影响

目的观察轻度过度通气下施行CO2气腹对呼吸和动脉血气的影响.方法行择期腹腔镜胆囊切除术(LC)病人术前快速诱导麻醉,气管内插管后行机械通气,吸入N2O、持续静脉输注异丙酚维持全麻,硬膜外间断给药.分别在诱导前5 min、气腹前1min和气膜后5、10、20、30、40、50、60min及放气后5 min记录各监测值,同时采桡动脉血作血气分析.结果气腹开始后20～60min,呼气末CO2分压(PETCO2)和Co2排出量(VCO2)较气腹前显著升高.气腹开始后,pH值逐渐降低,30 mm时较诱导前显著降低;PaCO2逐渐升高,60min时较诱导前显著升高,但PETCO2、VCO2、PaCo2及pH的变化均在正常范围.在气腹初期,气道压(PAW)较气腹前显著升高,而呼气分钟通气量(MVE)较气腹前明显降低.结论采用异丙酚静脉全麻复合硬膜外麻醉及气腹前适当过度通气的呼吸管理方式在LC中是切实可行的.     

2.5g/L罗哌卡因高位硬膜外阻滞对呼吸功能的影响

目的 观察2.5g/L罗哌卡因用于上胸段硬膜外阻滞时对呼吸功能的影响。方法 20例行择期乳癌改良根治术患者,于T3－4硬膜外腔注入2.5g/L罗哌卡因10－15ml,观察用药前及用药后10、15、30min4个时点的呼吸功能变化,同时监测麻醉平面和循环功能。结果 硬膜外腔注入2.5g/L罗哌卡因后10、15、30min与麻醉前相比,潮气量、补呼气量和肺活量明显降低（P＜0．05－0．01）,呼吸频率增快（P＜0．05）,分钟通气量与SpO2保持不变（P＞0．05）。胸部皮肤痛觉消失平面T1－2－T6－7,循环功能（HR、ECG、MAP、SBP、DBP）稳定。麻醉期间无其它不良反应。结论 2.5g/L罗哌卡因用于高位硬膜外阻滞,在获得满意镇痛范围及循环功能稳定的同时,肺通气功能基本保持不变。     

胸部创伤并发急性呼吸窘迫综合征的治疗

目的：总结胸部创伤并发急性呼吸窘迫综合征（ARDS）的临床特点。方法：对22例胸部创伤并发ARDS的患者进行分析;其中,肺叶切除术后6例,食管贲门癌术后10例,胸部严重外伤6例。救治方法主要包括去除病因,给予呼吸支持及循环支持等。结果：抢救成功18例,死亡4例。死亡原因主要是多器官功能衰竭及严重的肺部感染。结论：ARDS确诊后,应尽早应用机械通气治疗,其中包括使用呼气未正压通气、间歇正压通气等方法。     

直视下行大鼠气管插管的改良方法

目的 提高大鼠气管插管的成功率;方法 对比传统闭式法与改良直视法的成功率;结果传统闭式法的成功率为50％,改良直视法的成功率为100％。结论 改良直视法优于传统闭式法,值得推广应用。     

O2-sensing after carotid chemodenervation: hypoxic ventilatory responsiveness and upregulation of tyrosine hydroxylase mRNA in brainstem catecholaminergic cells

Ventilatory responses to acute and long-term hypoxia are classically triggered by carotid chemoreceptors. The chemosensory inputs are carried within the carotid sinus nerve to the nucleus tractus solitarius and the brainstem respiratory centres. To investigate whether hypoxia acts directly on brainstem neurons or secondarily via carotid body inputs, we tested the ventilatory responses to acute and long-term hypoxia in rats with bilaterally transected carotid sinus nerves and in sham-operated rats. Because brainstem catecholaminergic neurons are part of the chemoreflex pathway, the ventilatory response to hypoxia was studied in association with the expression of tyrosine hydroxylase (TH). TH mRNA levels were assessed in the brainstem by in situ hybridization and hypoxic ventilatory responses were measured in vivo by plethysmography. After long-term hypoxia, TH mRNA levels in the nucleus tractus solitarius and ventrolateral medulla increased similarly in chemodenervated and sham-operated rats. Ventilatory acclimatization to hypoxia developed in chemodenervated rats, but to a lesser extent than in sham-operated rats. Ventilatory response to acute hypoxia, which was initially low in chemodenervated rats, was fully restored within 21 days in long-term hypoxic rats, as well as in normoxic animals which do not overexpress TH. Therefore, activation of brainstem catecholaminergic neurons and ventilatory adjustments to hypoxia occurred independently of carotid chemosensory inputs. O2-sensing mechanisms unmasked by carotid chemodenervation triggered two ventilatory adjustments: (i) a partial acclimatization to long-term hypoxia associated with TH upregulation; (ii) a complete restoration of acute hypoxic responsivity independent of TH upregulation.     

心肌线粒体ATP敏感性钾通道开放保护线粒体结构和功能

目的　评价线粒体ATP敏感性钾通道 (mitoKATP)开放剂二氮嗪对缺氧心肌线粒体结构和功能的影响。方法　异丙肾上腺素 (ISO)皮下注射诱发大鼠心肌缺氧损伤 ,观察二氮嗪对线粒体呼吸控制比 (RCR)、膜流动性、磷脂酶A2 和磷脂含量的影响。结果　ISO皮下注射诱发大鼠心肌缺氧损伤后 ,与对照组比较线粒体RCR降低了 2 0 8% (P <0 0 1) ,膜流动性降低了 9 1% (P <0 0 5 ) ,磷脂酶A2 活性增加了14 4 5 % (P <0 0 1) ,磷脂含量下降了 37 5 % (P <0 0 5 ) ,二氮嗪预防性给药后可改善RCR、膜流动性和磷脂含量。结论　二氮嗪可保护心肌缺氧损伤后线粒体膜结构和功能的完整     

重度阻塞性睡眠呼吸暂停低通气综合征围手术期持续正压通气治疗

目的　观察重度阻塞性睡眠呼吸暂停低通气综合征 (obstructivesleepapneahypopneasyndrome ,OSAHS)围手术期病情变化和持续正压通气治疗 (continuouspositiveairwaypressure,CPAP)的影响 ,探讨围手术期治疗的必要性。方法　 45例重度OSAHS患者均接受了完整保留悬雍垂的改良悬雍垂腭咽成形术。其中 2 4例不做围手术期CPAP治疗的作对照组 ,2 1例行围手术期CPAP治疗 :术前CPAP治疗 7d以上 ,于术后 1～ 3d夜应用自动调节治疗压力的CPAP(autotitratedCPAP ,AutoSet)进行治疗。治疗组患者术后第二夜在AutoSet治疗下同时做多导睡眠监测 (polysomnography,PSG)。对呼吸暂停低通气指数 (apneahyponeaindex ,AHI)、最低血氧饱和度 (lowestSaO2 ,LSaO2 )、血压以及睡眠结构等指标进行观察。结果　对照组 2 4例患者中有 6例于术后第二夜LSaO2 比术前下降 ,AHI升高 ,另外 1 8例患者LSaO2 升高 ,AHI下降。治疗组 2 1例患者CPAP治疗前AHI为 (61 1± 9 9)次 /h( x±s,以下同 ) ,LSaO2 为 65 0 %± 9 6 % ,手术前CPAP治疗后AHI为 (2 2± 1 4)次 /h ,LSaO2 为 94 5 %± 2 9% ,t检验P <0 0 0 1 ;手术前经CPAP治疗临床症状消失。术后患者均能良好耐受AutoSet治疗 ,术后第二夜应用AutoSet治疗时AHI为 (3 6± 1 8)次 /h